Akinetic mutism

Akinetic mutism is a medical term describing patients tending neither to move (akinesia) nor speak (mutism). Akinetic mutism was first described in 1941 by Cairns et al. as a mental state where patients lack the ability to move or speak.[1] However, their eyes may follow their observer or be diverted by sound.[1] Patients lack most motor functions such as speech, facial expressions, and gestures, but demonstrate apparent alertness.[2] They exhibit reduced activity and slowness, and can speak in whispered monosyllables.[1][3] Patients often show visual fixation on their examiner, move their eyes in response to an auditory stimulus, or move after often repeated commands.[1][2] Patients with akinetic mutism are not paralyzed, but lack the will to move.[1] Many patients describe that as soon as they ‘will’ or attempt a movement, a ‘counter-will’ or ‘resistance’ rises up to meet them.[4]

Akinetic mutism varies across all patients. Its form, intensity, and clinical features correspond more closely to its functional anatomy rather than to its pathology. However, akinetic mutism most often appears in two different forms: frontal and mesencephalic.[2]

Akinetic mutism can occur in the frontal region of the brain and occurs because of bilateral frontal lobe damage. Akinetic mutism as a result of frontal lobe damage is clinically characterized as hyperpathic.[5] It occurs in patients with bilateral circulatory disturbances in the supply area of the anterior cerebral artery.[2]

Akinetic mutism can also occur as a result of damage to the mesencephalic region of the brain. Mesencephalic akinetic mutism is clinically categorized as somnolent or apathetic akinetic mutism.[5] It is characterized by vertical gaze palsy and ophthalmoplegia. This state of akinetic mutism varies in intensity, but it is distinguished by drowsiness, lack of motivation, hyper-somnolence, and reduction in spontaneous verbal and motor actions.[2][5]

Another cause of both akinesia and mutism is ablation of the cingulate gyrus. Destruction of the cingulate gyrus has been used in the treatment of psychosis. Such lesions result in akinesia, mutism, apathy, and indifference to painful stimuli.[7] The anterior cingulate cortex is thought to supply a "global energizing factor" that stimulates decision making.[8] When the anterior cingulate cortex is damaged, it can result in akinetic mutism.

Akinetic mutism can be misdiagnosed as depression, delirium, or locked-in syndrome, all of which are common following a stroke.[3] Patients with depression can experience apathy, slurring of speech, and body movements similar to akinetic mutism. Similarly to akinetic mutism, patients with locked-in syndrome experience paralysis and can only communicate with their eyes.[3] Correct diagnosis is important to ensure proper treatment. A variety of treatments for akinetic mutism have been documented, but treatments vary between patients and cases.

Treatments using intravenous magnesium sulfate have shown to reduce the symptoms of akinetic mutism. In one case, a 59 year old woman was administered intravenous magnesium sulfate in an attempt to resolve her akinetic mutism. The patient was given 500 mg of magnesium every eight hours, and improvement was seen after 24 hours. She became more verbal and attentive, and treatment was increased to 1000 mg every eight hours as conditions continued to improve.[11]

As seen in the case of Elsie Nicks, the puncture or removal of a cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst fills up again, the symptoms can reappear.[1]

Fourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic mutism by Cairns in 1941. She suffered from severe headaches her entire life and was eventually given morphia to help with treatment. She began to enter a state of akinetic mutism, experiencing apathy and loss of speech and motor control. A cyst on her right lateral ventricle was tapped, and as soon as the needle advanced toward the cyst, she let out a loud noise and was able to state her name, age, and address. After her cyst was emptied, she regained her alertness and intelligence, and she had no recollection of her time spent in the hospital. The cyst was drained two more times over the next seven months and was eventually removed. After eight months of rehabilitation, Elsie no longer experienced headaches or akinetic mutism symptoms.[1]